fkbp12(f36v)

Thalidomide-O-C6-NH2 hydrochloride (4-((6-aminohexyl)oxy)-2-(2,6-dioxopiperidin-3-yl)isoindoline-1,3-dione hydrochloride) is a synthesized E3 ligase ligand-linker conjugate.

EcDHFR/FKBP12 F36V binder-1 (compound 1) is a bifunctional molecule that integrates the domains of Escherichia coli dihydrofolate reductase (EcDHFR) and FKBP12F36V.

AP1867-3-(aminoethoxy) is a synthetic ligand for FKBP and can be used in the synthesis of PROTAC FKBP12 F36V degrader.

FKBP12 PROTAC dTAG-13 is a PROTAC and selective degrader that can be used for target validation during drug discovery by splicing FKBP12 F36V with CRBN and thereby degrading FKBP12 F36V.

AP1867 (FK506-binding protein) is a synthetic FKBP12 F36V-directed ligand attached to 320 substituted tetrahydrooxazepines (THOXs). AP1867 (FK506-binding protein) was synthesized via combined liquid- and solid-phase methods employing sequential Mitsunobu displacements followed by ruthenium-mediated olefin metathesis to close seven-membered rings; the resin-bound THOX ligands were coupled to AP1867 in parallel, yielding candidate heterodimerizers that demonstrated membrane permeability and bioactivity in human fibrosarcoma cells, facilitating the study of targeted protein interactions and intracellular modulation.

AP1867-3-(aminoethoxy) hydrochloride is a synthetic FKBP ligand based on AP1867 (a Ligand for Target Protein for PROTAC). It can be utilized in the synthesis of PROTAC-structured FKBP12 F36V degraders.

Degrader targeting mutant FKBP12F36V fusion proteins. Comprises a ligand selective for F36V single-point mutated FKBP12, a linker and a von Hippel-Lindau (VHL)-binding ligand. Induces potent and selective degradation of FKBP12F36V fusion proteins in vitro and in vivo. Selectively degrades FKBP12F36V-EWS/FLI fusion proteins and inhibits cell proliferation in FKBP12F36V-EWS/FLI-expressing Ewing sarcoma cells. Hydrochloride salt (Cat.No. 7374) available; suitable for in vivo use. Negative control dTAGV-1-NEG (Cat. No. 6915) also available. FKBP12F36V can be expressed as a fusion with a target protein of interest using genome engineering techniques, via transgene expression or CRISPR-mediated locus-specific knock-in. Custom knock-in cell lines for the dTAG and aTAG platforms are available from our sister brand R&D Systems. Email TPD@bio-techne.com to enquire. Plasmid vectors for the lentiviral expression and CRISPR-mediated knock-in of FKBP12F36V are available from Addgene.

dTAGV-1 TFA is a highly efficient, highly selective VHL-dependent PROTAC-mediated protein degrader that specifically targets and degrades mutant FKBP12 fusion proteins. dTAGV-1 TFA efficiently induces the degradation of FKBP12 fusion proteins at both the cellular and in vivo levels.

dTAGV-1-NEG TFA, a diastereomer, serves as the heterobifunctional negative control for dTAGV-1. It acts specifically as an FKBP12 F36V-selective degrader [1].

dTAG-47, a heterobifunctional molecule, specifically targets the mutant FKBP12 (FKBP12 F36V), which functions as a degradation tag (dTAG) when fused to a protein of interest. This compound is utilized in the study of basal-like breast cancers (BBC) [1].